Early growth and later atherosclerosis.

The concept that early growth has long-term biological effects is based on extensive studies in animals dating from the 1930s. More recently, compelling evidence for a long-term influence of early growth on later health has also emerged in humans. Substantial data now support the hypothesis that 'accelerated', or too fast infant growth, increases the propensity to obesity, glucose intolerance, raised blood pressure, dyslipidaemia and endothelial dysfunction, the clustering of risk factors which predispose to the development of atherosclerotic cardiovascular disease (CVD). The association between infant growth and these risk factors is strong, consistent, shows a dose-response effect, and is biologically plausible. Moreover, experimental data from prospective randomized controlled trials strongly support a causal link between infant growth and later cardiovascular risk. These observations suggest, therefore, that the primary prevention of CVD should begin from as early as the first few months of life. The present review considers this evidence, the underlying mechanisms involved, and its implications for public health.